E2F1-induced lncRNA, EMSLR regulates lncRNA LncPRESS1

E2F1 induces hundreds of protein-coding genes influencing diverse signaling pathways but much less is known about its non-coding RNA targets. For identifying E2F1-dependent oncogenic long non-coding RNAs (lncRNAs), we carried out genome-wide transcriptome analysis and discovered an lncRNA, EMSLR, which is induced both in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). EMSLR depletion blocks the cells in G1 phase and inhibits the clonogenic ability indicating that it is essential for the tumor-related phenotypes. We discovered that EMSLR represses the promoter activity of another lncRNA, LncPRESS1, which is located 6.9 kb upstream of EMSLR and they display an inverse expression pattern in lung cancer cell lines. Depletion of C-MYC results in downregulation of EMSLR and simultaneous upregulation of EMSLR target LncPRESS1, exemplifying how C-MYC and E2F1 signal transduction pathways control the network of lncRNA genes to modulate cell proliferation and differentiation.

Automated summary

E2F1 induces the expression of lncRNA EMSLR in lung adenocarcinoma and lung squamous cell carcinoma, and it is involved in regulating cell proliferation and differentiation signaling pathways. EMSLR functions by repressing the promoter activity of LncPRESS1, and C-MYC plays a role in the regulation network of EMSLR and LncPRESS1.